Nursing care plan craniocerebral trauma


I. Pathophysiology
a. Craniocerebral trauma, also called traumatic brain injury
(TBI), acquired brain injury, head injury—Physical injury to
the cranium and intracranial structures with varied outcomes,
ranging from no apparent (or a temporary neurological)
disturbance to permanent impairment of brain function,
including persistent vegetative state or even death depending
on the extent of the damage
b. TBI may be open or closed and can include brain concussion,
contusion, laceration, hemorrhage, or skull fractures.
i. Concussion: most minor and most common form of head
ii. Intracranial hemorrhage: defined by the region of the
brain (intracerebral) or surrounding structures affected,
such as subdural, epidural, subarachnoid, brainstem
1. Intracerebral hemorrhage: may occur along with other
brain injuries, particularly contusions, with signs and
symptoms dependent on the size and location and
may be apparent immediately or develop slowly
(Zink, 2005).
2. Acute subdural hematoma: caused by venous bleeding
when bridging veins are torn, occurring in 5% to 25%
of all severe head injuries involving a contusion or
laceration and often accompanying intracerebral
bleeding (Reddy, 2006); signs and symptoms present
almost immediately and increase rapidly.
3. Epidural hematoma: arterial bleeding usually from the
middle meningeal artery in the temporal region, typically
manifested by a brief loss of consciousness at the
time of trauma, then a lucid interval, which may last
for several hours; between 30% and 50% of individuals
incur neurological deterioration (Reddy, 2006).

II. Etiology
a. Primary injury (Zink, 2005)
i. Penetrating injury: Object forcibly enters the cranial
vault, damaging the protective meningeal layers, cerebral
blood vessels, and brain tissue.
ii. Contact phenomena injury: Object strikes the head,
resulting in concussion, cerebral contusion, skull fracture,
or intracranial hemorrhage.
iii. Acceleration-deceleration injury: Brain rapidly accelerates
and decelerates within the skull, causing the brain
to strike the skull, usually in the front and the back of
the skull, causing tearing of neuronal tissue and cerebral
blood vessels.
iv. Rotational acceleration-deceleration injury: Forces
cause the brain to twist within the skull, resulting in
torsion and shearing of nerve tissue and blood vessels.
b. Secondary brain injury (Granacher, 2003)
i. Thought to involve inflammation and the natural process
of programmed cell death (apoptosis).
ii. Diffuse axonal injury: shearing injury of large nerve
fibers (axons covered with myelin) in many areas of the
brain, or stretching or shearing of blood vessels from
the same forces, producing hemorrhage
iii. Systemic or neurological complications can also cause
or exacerbate secondary brain injury—hypotension,
hypoxia, hypercapnia, intracranial hypertension,
acid-base imbalance, cerebral vasospasm, electrolyte
abnormalities, hyperthermia, infection, cerebral
ischemia, seizures, and hypoglycemia or hyperglycemia.
c. Leading mechanism for TBI in the United States:
(Langlois, 2004)
i. Falls: 28%, highest for children aged 0 to 4 and those
aged 75 or older
ii. Motor vehicle-traffic crashes: 20%
iii. Struck by or against: 19%, which includes sports-related
iv. Assaults: 11%, including firearm use
v. Gunshot wounds: most common penetrating injury and
most deadly cause of TBI in clients under age 35
(Zink, 2005)
vi. Blasts: leading cause of TBI for active duty military
personnel in war zones (Defense and Veterans Brain
Injury Center, n.d.)

III. Statistics (Centers for Disease Control and Prevention
[CDC], 2006)
a. Morbidity: 1.4 million people sustain a TBI annually in the
United States, 1.1 million are treated and released from an
emergency department, 235,000 are hospitalized; approximately
2% of the U.S. population currently have a longterm
or lifelong need for help to perform activities of daily
living as a result of a TBI (Thurman et al, 1999).
b. Mortality: There are 50,000 deaths annually.
c. Cost: Direct medical costs and indirect costs, such as lost
productivity of TBI, totaled an estimated $60 billion in the
United States in 2000 (Finkelstein, 2006).

Care Setting
This plan of care focuses on acute care and acute inpatient
rehabilitation. Brain injury care for those experiencing moderate
to severe trauma progresses along a continuum of care,
beginning with acute hospital care and inpatient rehabilitation
to subacute and outpatient rehabilitation, as well as
home- and community-based services.

Related Concerns
Cerebrovascular accident (CVA)/stroke
Psychosocial aspects of care
Seizure disorders
Surgical intervention
Thrombophlebitis: deep vein thrombosis
Total nutritional support: parenteral/enteral feeding
Upper gastrointestinal/esophageal bleeding

Nursing Priorities
1. Maximize cerebral perfusion and function.
2. Prevent or minimize complications.
3. Promote optimal functioning/return to preinjury level.
4. Support coping process and family recovery.
5. Provide information about condition, prognosis, potential
complications, treatment plan, and resources.

Discharge Goals
1. Cerebral function improved; neurological deficits resolving
or stabilized.
2. Complications prevented or minimized.
3. Activities of daily living (ADLs) met by self or with
assistance of other(s).
4. Family acknowledges reality of situation and involved in
recovery program.
5. Condition, prognosis, complications, and treatment regimen
understood and available resources identified.
6. Plan in place to meet needs after discharge.

This entry was posted in Cario Cerebral Trauma and tagged , , , . Bookmark the permalink.

Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.